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Wedge-shaped medullary lesions in multiple sclerosis.Qiu W, Raven S, Wu JS, Carroll WM, Mastaglia FL, Kermode AG.SourceCentre for Neuromuscular and Neurological disorders, University of Western Australia, Australia.AbstractMultiple sclerosis (MS) is a heterogeneous disease with variable clinical features and magnetic resonance imaging (MRI) findings. We report four MS cases with unusual wedge-shaped lesions in the paramedian ventral medulla oblongata demonstrated on MRI. The clinical features and MRI characteristics of the medullary lesions suggest an impairment of venous drainage. We propose that the formation of these wedge-shaped lesions may be related to the pattern of venous drainage in the ventral medulla and raised venous pressure due to chronic cerebrospinal venous insufficiency which has recently been described in MS.

One of the doctors on the forefront of imaging this process is Dr. Mark Haacke--

Haacke has been working with researchers throughout the world for more than five years applying his techniques specifically to traumatic brain injury, stroke, Parkinson's disease and multiple sclerosis. In this current project, he has demonstrated that there is a lower impact load, either inertia or direct impact forces, which may damage only veins, and he has shown medullary vein damage that has not been visualized with other techniques. The medullary veins drain the frontal white matter of the brain, so reduced blood flow here could possibly impair the higher level frontal neurocognitive functions. In light of this, treatments that improve blood flow to the brain might be a promising direction to pursue.

We could be there so quickly. If neurovascular contact between the veins, medulla and surrounding nerves can be proven and corrected through angioplasty or atlas therapies, the 'syndrome' could be renamed to something more intriguing to the neurologists. NVCMVGVNS-Neurovascular Contact of Medulla, Vagus, Glossopharyngeal, and Vestibulocochlear Nerves Syndrome. LOL Maybe someone else should name it...if it actually exists.

Being the completely non-medical person I am, and sometimes catching myself arguing the wrong side of what should be completely obvious, I wonder if medical professionals who know better aren't reading what I write for the occasional giggle.

They're welcome to I guess.

Pressure wants to go somewhere, and the more of it, the more likely it is to cause expansion if that path is of the least resistance. Will the pressure increase be absorbed by compliant vein walls, or go back upstream? I think I have seen images of a refluxing stream of blood in the middle of a stream going in the opposite direction, and I would have thought that could only happen by convection, in very slow-moving stream. It might depend on how reflective the obstruction is.

It makes me wonder, how far outside the normal range of pressures must it be for this to occur? Said another way, if the pressure vector in the middle of a vein is stronger that the vector flowing opposite, momentarily, will this perhaps cause a momentary upstream flow? (I.e. a "back-jet"?)

I suggest that pulsatile changes in pressure may weaken the vessel walls, over time, similar to the "metal fatigue" in airplanes, only in this case causing them not to rupture, but to become dangerously porous (especially at weak points, which may coincide with places where turbulence is greater). With the waves of rhythmic breathing, there may by periodic waves of back-pressure superimposed on the pulses.

To completely avoid getting quantitative, you might consider that it is really the deltas in pressure, that are more relevant than the absolute value. Also, the range of normal pressures (i.e., the values that will not cause reflux or vessel dilation which could lead to fatigue) might be significantly smaller, because their average value is much smaller than the average arterial pressure, either systolic or diastolic. So that would make veins more sensitive to abnormal pressure changes than arteries. Combined with the relative thinness of vein walls to arterial ones, even more so in the brain for some reason, the brain region might more likely experience these problems than other places.

Certainly it is the only place where a BBB is important.

These vessels on the venous side get progressively smaller as they approach the BBB. Perhaps some diameter of vessel (like the widest diameter of venules), perhaps also co-located with weaker and more turbulent spots, is more vulnerable than others, simply because of the size of particles that the flow is carrying at those points? Could this be why there are lesions there? And somewhere nearby to that might be the reason that the BBB itself becomes more porous?

Fibrinogen: could that also be why lesions are fibrous? And is this fibrousness related to the morphology when collagen changes?

cheerleader wrote:...One of the doctors on the forefront of imaging this process is Dr. Mark Haacke--

Haacke has been working with researchers throughout the world for more than five years applying his techniques specifically to traumatic brain injury, stroke, Parkinson's disease and multiple sclerosis. In this current project, he has demonstrated that there is a lower impact load, either inertia or direct impact forces, which may damage only veins, and he has shown medullary vein damage that has not been visualized with other techniques. The medullary veins drain the frontal white matter of the brain, so reduced blood flow here could possibly impair the higher level frontal neurocognitive functions. In light of this, treatments that improve blood flow to the brain might be a promising direction to pursue.

...cheer

Your additional emphasis might be ambiguous. "A lower impact load" seems to mean, a lower threshold where an impact "may damage only veins". In other words, he has demonstrated that veins may be the weak point and may be more sensitive than arteries, when an impact occurs. Maybe they are also more sensitive to changing or aberrant pressures? That could be seen as evidence of part of what I was talking about, with respect to pressure and lesions in my post. Part of what I was saying was trying to get at why they are weaker, in cases of BBB, and lesion damage (diameter/particle size, turbulence, vessel thickness). He seems to have added iron and oxygen content to the list. I personally think everything points to a venous problem, the source of which can be an impact, as well as several others.

When will the penny drop? Or the other shoe? Is that why some people wear pennies on their shoes?

1eye wrote:Being the completely non-medical person I am, and sometimes catching myself arguing the wrong side of what should be completely obvious, I wonder if medical professionals who know better aren't reading what I write for the occasional giggle.

I am sure the medical people do laugh at our ponderings. I even laugh at my own. But many amazing medical and scientific discoveries were found by clumsy accident or random epiphany. Penicillin was an accident. A falling apple gave us "gravity." Lazily watching a ship travel over the horizon led to the knowledge the earth isn't flat. (folk tales some of these?) We might just come up with something good if we keep poking away.

As for the rest of your posts here, I haven't yet bought the idea that flow issues cause all or even a good number of the lesions and damage in MS. Flow issues are likely a part of the complete MS presentation in some people, but something else is causing most of the lesions. Something else is causing the random attacks in RRMS. Something else is continuously wrong in SPMS and PPMS. The most striking and common improvements observed from CCSVI intervention can't be attributed to the cessation of BBB failure due to venous pressure issues. I'm still reading your posts though in case you might convince me. You don't happen to be an engineer, do you?

Having just been unsuccessfully argued out of my position on lesions and the BBB, I am unlikely to tell you whether or not I am an engineer. Let's just say I think quite highly of Dr. Haacke, and I like numbers, even when I don't have any on me.

My recent experiences with venous issues, along with my simultaneous new/old symptoms, makes me feel even more strongly that venous fluid pressure and possibly CSF/venous fluid dynamics are at the root of this. Happens when I wear my new compression stockings. I don't necessarily believe there is such a thing as "MS". I will in all likelihood go to my grave believing that there isn't anything like what has been described to explain the state I'm in.

As for the rest of your posts here, I haven't yet bought the idea that flow issues cause all or even a good number of the lesions and damage in MS. Flow issues are likely a part of the complete MS presentation in some people, but something else is causing most of the lesions. Something else is causing the random attacks in RRMS. Something else is continuously wrong in SPMS and PPMS. The most striking and common improvements observed from CCSVI intervention can't be attributed to the cessation of BBB failure due to venous pressure issues. I'm still reading your posts though in case you might convince me. You don't happen to be an engineer, do you?

Aside from their apparent disdain for the humanities (most apparent in the young), I think Engineers are among the best and most practical scientists around, and I am on their side.

"The most striking and common improvements": where did they come from, if not directly as a result of changes to the venous flow during and after the PTA procedure, ballooning obstructions, narrowings, and bad valves in veins?? Tickling the vagus? Placebo?

The attacks don't seem very random to me. The improvements are immediate in many cases, which to me is best explained by the immediate improvements in oxygen distribution and fluid pressure. I don't think that anything other than thresholds of ability, employ-ability, and care costs are involved, in the distinctions between "rr", "sp" and "pp". It's an actuarial and legal convenience, very effective for subdividing the workload. I've known people with all of them, at many ages.

Many problems start life as intermittent, get worse, and end up continuous, until total failure: from plumbing, to wiring, to lighting, to car engines. Why should CCSVI be any different? When you think about it, it's pretty miraculous that humans last as long as they do without these kinds of malfunctions.

I didn't mean the engineer remark to be an insult in any way. My dad was your typical engineer, my husband an atypical. I hung out with ME's, EE's, and ChemE's in college. I like engineers! Your reasoning and focus just remind me of my dad's. He had a very different way of thinking than I do and for me, trying to understand his reasoning was sometimes difficult. We processed things so differently communicating with each other was like trying to communicate with an alien for both of us. You've tied my brain in knots several times and it's not for my lack of intelligence. If you aren't an engineer, maybe you should consider engineering as a career option. That's a compliment!

An example of this difference in thinking...

Having just been unsuccessfully argued out of my position on lesions and the BBB, I am unlikely to tell you whether or not I am an engineer.

The logic escapes me but I am sure it makes perfect sense to you. Is that knowledge only to be rewarded if someone successfully changes your mind about your theory that CCSVI is the cause of all BBB failure in MS? Reminds me of Rumpelstiltskin and then I start thinking about alchemy and whatnot. See, that's the crazy place you make my brain go with your alien engineer-like thinking.

The most striking and common improvements": where did they come from, if not directly as a result of changes to the venous flow during and after the PTA procedure, ballooning obstructions, narrowings, and bad valves in veins?? Tickling the vagus? Placebo?

My theory is that the improvements from CCSVI intervention can be attributed to elimination of NVC between the veins, the medulla and surrounding nerves. Throughout my numerous ramblings, you should probably find evidence of NVC and inhibited nerve and medulla function. It is obviously an unproven theory. But it's not a bad theory being that it would explain all of the near instantaneous improvements.

The attacks don't seem very random to me. The improvements are immediate in many cases, which to me is best explained by the immediate improvements in oxygen distribution and fluid pressure. I don't think that anything other than thresholds of ability, employ-ability, and care costs are involved, in the distinctions between "rr", "sp" and "pp". It's an actuarial and legal convenience, very effective for subdividing the workload. I've known people with all of them, at many ages

Truth be told, I don't think the attacks are random. I think they are the result of stress induced cortisol/aldosterone surge...which can happen randomly depending on an individual's experiences, lifestyle, diet, yadda yadda. Once you get to SPMS or PPMS, the parts of the brain that are responsible for negative feedback on hpa axis activation are so damaged there is no stopping the ever-worsening hyperactivation.

Many problems start life as intermittent, get worse, and end up continuous, until total failure: from plumbing, to wiring, to lighting, to car engines. Why should CCSVI be any different?

So goeth the plumbing, the wiring, the lighting, the car engines, the jugulars, the cbf and the csf, so goeth the hippocampus and hpa axis.

Anonymoose wrote:I didn't mean the engineer remark to be an insult in any way.

I didn't take it as an insult. I might have meant you were unlikely to convince me it was relevant. I suppose the explanation might be that ad-hominem arguments bother me. So does being told my reasoning is somehow strange or unusual. No little green men here, rumpled or not.

Don't take it personal. I won't argue against your profession, either, even if you are a neurologist. I would let one mow my lawn, etc., etc. Some of my best friends are cataloguers.

Only some of my attacks have been triggered by stress. I think other things are equally harmful as triggers (maybe some even happen during sleep). Stress is just one. The result is always that that the BBB, and stuff on both sides of it, gets damaged, even killed.

We know fibrinogen damages nerves, and is a normal blood component. Does stress improve its chances of crossing into the CNS? All I know is it makes vessels shrink. Are they then more likely to leak more fibrinogen? Is fibrinogen being released locally in response to local damage of other origins, to blood vessels?

So goeth the plumbing, the wiring, the lighting, the car engines, the jugulars, the cbf and the csf, so goeth the hippocampus and hpa axis.

Whew, I thought you would say some get an unrelenting progression. To me that is like a well that starts out dry, or a light bulb dying without ever flickering back on. Stuff happens; I've seen it.

But I don't have "a theory that CCSVI is the cause of all BBB failure in MS". Just a heck of a lot of it... I have no theories. Just words, often repetitions to which I can claim neither credit nor blame. And many questions. Couldn't reflux, hypoxia, large numbers of free radicals, venous pressure, also be causes, as well as stress hormones? Even if stress was always the smoking gun, those things will cause further problems (including autoimmune attacks), once the BBB is breached.

Oh bother. I made no ad hominem argument and to me, alien doesn't have a negative connotation either. Heh. That must mean I am alien. Thank the Lord...I'd hate to be standard human issue and I'd hate to live in a world with standard issue humans. I think you misunderstand me (or my intentions) as much as I misunderstand you. Bygones.

A peace offering...This is an interesting read. Speaks of intracranial pressure and increased risk of BBB breach. Could this somehow support the blood flow irregularity induced BBB breach? I looked up MS and increased ICP and there was no absolute connection between the two. That doesn't mean that it can't play a part in those folks with CCSVI. Does CCSVI cause increased ICP? How?http://neuroanesthesia.ucsf.edu/residen ... oncept.pdf

I think excess aldosterone causes increased immune activity and endothelial dysfunction which creates BBB breach, allowing the immune system and fibrinogen do it's work where it's not meant to do so. Aldosterone levels can be influenced by not only stress but also the performance of cortisol's negative feedback loop, sodium, potassium, magnesium, vitamin D, and drug intake to name a few. HPA axis dysregulation is one thing that all pwms have in common. The alternate causes you listed are not issues with all pwms. I might be wrong, but it won't stop me from being stubborn and trying to treat HPA axis dysregulation as the cause to see what happens.

Anonymoose--When there's new research on CCSVI/blood brain barrier/endothelium, someone will post it on this forum.The search function is a really great feature of this site. Trust me, all of the vascular/MS papers in pubmed end up here on the CCSVI forum, like the one you linked which began this thread.

It's probably a good idea to see what's been discussed, and if you're interested, post and "bump" one of these threads. That way, the discussion can pick up where it left off, and the work of other people can be recognized. 1eye was recognizing many of the theories that have been explored regarding the breakdown of the blood brain barrier and the cerebral endothelium.

If you have new papers on your theory of the HPA axis, by all means share. But that might be best in the general forum, not on the CCSVI forum.Here are some rather long threads on this topic you might enjoy. They were posted in the general forum.From Odd Duck--2005 -HPA Axis and MSpost6123.html?hilit=HPA%20axis#p6123An incredible post from Shayk--2007--on cortisol, inflammation and neurodegenerationpost25290.html?hilit=HPA%20axis#p25290

Wow. That makes the process of sharing information and thoughts quite cumbersome. I didn't realize people felt proprietary towards the studies and ideas they posted here. My apologies if I have offended anyone by reposting a study they discovered or an idea they shared unbeknownst to me.

As for my comments on hpa axis regulation, those were my answers to questions 1eye asked in this thread. I didn't think it necessary to start a new post to answer his questions.

Thankfully, my curiosity about ccsvi has been quenched. I won't be breaking anymore protocol rules...in this forum.

Anonymoose wrote:Wow. That makes the process of sharing information and thoughts quite cumbersome. I didn't realize people felt proprietary towards the studies and ideas they posted here. My apologies if I have offended anyone by reposting a study they discovered or an idea they shared unbeknownst to me.

As for my comments on hpa axis regulation, those were my answers to questions 1eye asked in this thread. I didn't think it necessary to start a new post to answer his questions.

Thankfully, my curiosity about ccsvi has been quenched. I won't be breaking anymore protocol rules...in this forum.

As you were.

I must have missed that thread about protocol rules. Sorry. I didn't mean to break anybody's concentration or interrupt anything. I think this is an interesting discussion and I do not mind finding it here, though I should probably look at other treatments. The reason I don't mind, is I am not a person who frequently reads the main Forum. I credit cheerleader for doing that, though, even though she is not a patient herself. I do understand why anyone gets more reading done than I do, and why they have more energy.

It is starting to look to me like BBB damage/increased porosity is the main unknown, and folks are down to discussing what is the most likely reason for it in the majority of cases. Maybe if that were universally recognized (as surely it must have been by the makers of Tysabri), well, we might have more agreement and fewer misunderstandings, anyway, I don't know.

The source of the idea that I have any theories I can call my own might be that I am so seldom found anywhere else. I don't get out enough.

I am too sensitive perhaps when asked about my occupational vocation, because for one thing you are reading it, for the most part. Sad, isn't it? Honestly, I had a life, but I seem to have mislaid it. A reward is offered for any information on its whereabouts.

I am too sensitive perhaps when asked about my occupational vocation, because for one thing you are reading it, for the most part. Sad, isn't it? Honestly, I had a life, but I seem to have mislaid it. A reward is offered for any information on its whereabouts.

Oh 1eye, don't be sad about that. Your life is different but it hasn't been mislaid. Our value isn't based on our vocations. Our value is based on what we do with what we have and from what I can see, you do a lot. We all appreciate your contributions and insights. I would miss you if you weren't here! So take some pride in what you do!

I wish you peace and joy...whilst I await another wrist slap for going off topic again.

anonymoose wrote--I am sure the medical people do laugh at our ponderings. I even laugh at my own. But many amazing medical and scientific discoveries were found by clumsy accident or random epiphany. Penicillin was an accident. A falling apple gave us "gravity." Lazily watching a ship travel over the horizon led to the knowledge the earth isn't flat. (folk tales some of these?) We might just come up with something good if we keep poking away

1-eye wrote--

I must have missed that thread about protocol rules. Sorry. I didn't mean to break anybody's concentration or interrupt anything. I think this is an interesting discussion and I do not mind finding it here, though I should probably look at other treatments. The reason I don't mind, is I am not a person who frequently reads the main Forum. I credit cheerleader for doing that, though, even though she is not a patient herself. I do understand why anyone gets more reading done than I do, and why they have more energy.

It is starting to look to me like BBB damage/increased porosity is the main unknown, and folks are down to discussing what is the most likely reason for it in the majority of cases. Maybe if that were universally recognized (as surely it must have been by the makers of Tysabri), well, we might have more agreement and fewer misunderstandings, anyway, I don't know.

The source of the idea that I have any theories I can call my own might be that I am so seldom found anywhere else. I don't get out enough.

I am too sensitive perhaps when asked about my occupational vocation, because for one thing you are reading it, for the most part. Sad, isn't it? Honestly, I had a life, but I seem to have mislaid it. A reward is offered for any information on its whereabouts.

to me -- this says a lot. you guys were having a good discussion--more in laymens terms. i to do not visit everything here at tims--it's hard when limited. so, if we double up on something i don't think it will hurt awhole lot. and, as anonymoose said "we might come up with something good that we keep poking around." REMEMBER the BRAINEACS" that named these symptoms they call ms and threw us all into one basket and want to treat us with a drug that fits all. So, with that thought we keep in mind the ccsvi the csf etc. is not gonna be a straight shot. following the trail of ccsvi alone has proven to have many speed bumps, detours, erosions, to try to get to the destination wanted. and, we do need the BRAINEACS too. but, a patient should never be underestimated. we're living it, we are individuals thinking out of the box.

thx for all your posts.---and 1-eye, i do understand the "had a life" thing. i have said--i know i had a life--but i got abducted--and i'm waiting for the spaceship to find me and take me back.

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